And so ME Research UK is 10 years old…
A decade might seem a long time, but
it is only a twinkle of an eye in the life of a
charity. The most perilous years for
newborn charities, so they say, are the
first five and many fail at this early stage.
The ones that survive continue to grow
slowly, building up a bedrock of support
and increasing in credibility year-on-year
for 20, 30 or 40 years. That’s why the
most successful charities tend to be the
longest established.
There’s an old saying that the best
way to realise just how far you’ve
travelled is to look back; so how far has
ME Research UK come in ten years? Well,
in that time the charity has provided
funding for 29 projects, most over the
past 6 years. It’s sobering to think that ME
Research UK, comparatively small as
research charities go, has funded more
specific research projects on ME/CFS than
any other single organisation in the world
outside the American continent.
Without our impetus or funding
(alone or with partners) most of these
projects would never have taken place.
For instance, Prof. Julia Newton’s
research on autonomic dysfunction at the
University of Newcastle would not have
begun and flourished into the much larger

programme we see today (see page 6);
and the Vascular and Inflammatory
Diseases Research Group at the
University of Dundee would not have
uncovered a range of abnormalities in
oxidative stress, apoptosis and arterial
stiffness (page 8). Similarly, Prof. Nijs’
programme in Belgium on exercise,
immunology and its consequences; Dr
Jonathan Kerr’s investigations of gene
snips or comparative genetic signatures;
and single investigations, such as the
explorations of retrovirus in Swedish
patients (page 15) or the experience of
pain in Scottish patients (page 4) would
not have been instigated or completed.
Yet we have had a wider, more
diffuse influence than simply funding
specific projects; after all, our mission is
to ‘energise research’ and bring the need
for scientific investigation of ME/CFS to
the attention of government and
professional groups. For example, our
chairman, Dr Vance Spence, has given
some 58 lectures to a variety of audiences
over the decade, and we have been in
regular contact with a range of research
groups to try to stimulate new research;
indeed, the projects we have funded are
far fewer than those we have tried to get
off the ground, and are only a tiny
proportion of those we should like to see
commissioned. Also, each year we answer
queries from around 400 people by
telephone and e-mail in our efforts to
provide helpful information and broadcast
research findings widely.
The fact that we are one of only a
handful of organisations in the entire
world funding biomedical research into
this illness reminds us of the long journey
ahead. In its 10 years ME Research UK
has made an enormously valuable
contribution; we now need your
continued support to take our research
agenda forward into the next decade and
beyond.
Dr Neil Abbot
Operations Director
ME Research UK

this issue
Experiences of pain in ME/CFS.......................4–5
How patients describe their pain, its location and its impact

Abnormalities in muscle..................................6–7
A Newcastle study looking at acid handling in muscle after exercise

Biochemical abnormalities in children.........8–10
Do children with ME/CFS have the same vascular abnormalities as adults?

Anniversary special......................................11–14
A celebration of 10 years of ME Research UK

XMRV: the plot thickens...................................15
What’s happened since the first reports of the virus

Experiences of
Pain is a very common symptom in
ME/CFS; it tends to be experienced in the
muscles and/or joints, but it can often be
widespread and changeable in location
and intensity. In one survey, quoted in the
Chief Medical Officer’s report, 79% of
patients said that they had severe pain
sometimes, much of the time, or all of the
time, and between 84 and 94% of patients
in formal research studies report some
degree of muscle or joint pain.
Importantly, 53% of unemployed people
surveyed recently by the campaigning
charity Action for ME
said that chronic
pain was one of
the greatest
barriers to their
obtaining paid
employment.
Despite this,
there is very little
scientific
information about the specific pain
characteristics of ME/CFS patients. What
kind of pain is it? Where is it localised?
What strength is it? To explore such
questions, ME Research UK provided
part-funding for a PhD studentship, under
the supervision of Prof. Lorna Paul and Dr
Les Wood (pictured on page 13), at
Glasgow Caledonian University. The
student, Rebecca Marshall, has now
submitted her thesis, and the first
scientific paper from her work has just
been published in the Journal of
Musculoskeletal Pain.
For the investigation, 50 people with
ME/CFS and painful symptoms were
recruited from support groups across
Scotland; all had previously been
diagnosed by a consultant or general
practitioner, and all met the CDC-1994
and Canadian Guideline symptom criteria.
No participants had any psychiatric illness
or any other serious conditions such as
cancer, rheumatoid arthritis or multiple
sclerosis (which would have affected their
experience of pain).
The investigators visited the patients
in their own homes to conduct their
interviews, which allowed the

participation of those who were so
severely affected that they would not have
been able to make a trip to the hospital.
This was particularly important in this
study since the researchers wanted to
ensure that the findings represented the
full spectrum of ME/CFS. Between 10%
and 25% of ME/CFS sufferers fall into the
“severe” category, so 10 of the 50
patients interviewed by Dr Paul’s team
were either housebound or bedbound
and had been recruited via the national
charity, the “25% ME Group” which
caters for severely ill
patients.
Overall, the 50
patients had been
ill for an average
of 12.6 years
(range 1.3 to
27.4), and only
one was working
full time, and two
part-time. A number of tools and
questionnaires were used to evaluate
participants’ experiences of pain,
and these consisted of a visual
analogue scale, the Margolis
Body Chart, the McGill Pain
Questionnaire, the Pain
Anxiety Symptoms Scale-20
and the Medical Outcome
Survey Short Form-36 (see
opposite for more detailed
descriptions of each of these).
The results revealed that
pain is indeed an important
symptom of patients
with ME/CFS. The
most common
painful symptom
was muscle pain,
which was
reported by more
than two-thirds of
patients. The
average intensity
of pain at the
time of the
interview was
reported to be
around 43 out of

Muscle pain was
reported by more than
two-thirds of patients
with ME/CFS

4 • BREAKTHROUGH • Autumn 2010

Pain
a maximum of 100 mm on the visual
analogue scale, while the average intensity
over the previous 24 hours was higher at
around 58 mm. The investigators suggest
that this latter value may be a more
accurate reflection of patients’
experiences, particularly if pain fluctuates.
Significantly, ME/CFS patients reported
worse pain than did patients with
rheumatoid arthritis or multiple sclerosis
in previous studies, both conditions in
which pain is recognised as a major
symptom.
Patients used words such as
“throbbing”, “aching”, “tender”,
“gnawing” and “burning” to describe the
pain they experienced, while those with
more severe illness also used “exhausting”
and “nagging”. In fact, as the
chart opposite shows, only the
severe patients chose the
word “gruelling” while

none chose the less emotive words
“tight” or “annoying” — indicating more
severe pain, and intensity, in the most
severely affected group.
These descriptions may give clues as
to the mechanisms causing pain in
ME/CFS; in particular, “burning” pain is
often associated with neuropathic
conditions in which the nerves have been
damaged. Also, they may help in assessing
any change in the quality of pain over
time, such as after treatment, as Dr Paul’s
group suggests. Despite this burden of
pain, most participants described their
mood as generally positive, although those
with more intense pain tended to
describe a lower mood.
The most common locations of pain
were the cervical spine (in 66% of
patients), the anterior thighs (44 to 46%),
the lumbar spine (42%) and the posterior
calves (38%), and most participants had
pain in more than one location. Nearly a
third of patients said they experienced
their most severe pain in the area of the
cervical spine/upper trapezius, while 20%
reported the scapular/upper thoracic area
and another 20% reported the right
lumbar spine as the most painful regions.
Twenty-eight participants said they
experienced the worst pain in the
morning, while it was the afternoon for
four individuals, the evening for ten and
the night for eight.
The results of the Pain Anxiety
Symptoms questionnaire suggest that the
study participants were not overly
anxious or fearful because of their pain,
although the most severely affected were
more susceptible. When considering
quality of life, Dr Paul’s findings were
similar to those of Dr Gwen Kennedy’s
study from 2004 (published in the Annals
of Epidemiology). Patients tended to have
reduced physical functioning and vitality
(but not emotional or mental health), and
again this was more pronounced in those
with more severe illness.
This is the first major study to
document and categorise the pain
experienced by people with ME/CFS, and
to provide sound, objective, scientific
support to their anecdotal and clinical
reports of painful symptoms. As the
authors say, “This study has emphasised
that the problem of chronic pain… needs to
be treated as seriously as the pain
experienced in other conditions such as
rheumatoid arthritis and multiple sclerosis.”

Margolis Body Chart
Participants use a diagram of the human body to indicate the areas in which they
experience the most pain. This is then matched to a chart which divides the body
into 45 sections, in order to identify the locations of most pain.

McGill Pain Questionnaire
Participants are asked to describe their pain using words from a standard list of
78, grouped into 20 subcategories. Numerical values are assigned to each word,
and a Pain Rating Index is calculated as the total of the values for each word
chosen. This provides a measurement of the pain itself (sensory component), as
well as unpleasant feelings and emotions (affective component), and how it is
judged by the sufferer (evaluative component).

Pain Anxiety Symptoms Scale-20
Participants are asked to score their experience of 20 psychological aspects of
pain, such as anxiety, fearful thinking, feelings of wanting to escape or avoid a
situation, and physiological responses. Each item is scored from 0 (never) to 5
(always), and the total is calculated out of a maximum of 100.

Medical Outcome Survey Short Form-36
A questionnaire consisting of 36 questions examining physical functioning, physical
role, bodily pain, general health, vitality, social functioning, emotional role and
mental health. The participant’s answers to each question are translated into a
total score from 0, representing poor health, to 100, representing good health.

Autumn 2010 • BREAKTHROUGH • 5

Abnormalities in Muscle
The autonomic nervous system has a
range of important functions, so the
consequences can be severe when
it goes wrong. Since ME/CFS
patients experience symptoms
such as dizziness, altered vision,
nausea and fatigue when they are
standing, particularly when they
are standing still, the possibility
exists that the autonomic
nervous system could be at
fault.
Since 2006, with the
financial help of ME
Research UK, Professors
Julia Newton and David
Jones (pictured) of the School
of Clinical Medical Sciences,
University of Newcastle, have
examined a large group of patients
using a battery of tests of autonomic
function, including heart rate and blood
pressure. In a series of fascinating
scientific papers, they have reported
finding autonomic dysfunction in
three-quarters of ME/CFS patients, a
most unexpected result; they have
shown that the heart rate response
to standing is abnormal in a
significant proportion of patients; and
they have confirmed that blood pressure
is lower, and blood pressure regulation
abnormal, in this clinical group compared
with healthy people.
The autonomic nervous system also
plays a part in regulating events in
exercising muscle, however, and the
researchers hypothesised that it
might be involved in the
exercise-induced symptoms so
characteristic of ME/CFS. To
examine this, they enlisted the
help of phosphorus magnetic
resonance spectroscopy (MRS),
a marvelous tool which allows
assessment of acid (pH) handling
inside the muscle where the
problems might lie.
Sixteen ME/CFS patients
and healthy controls matched
for age and sex underwent MRS
to examine acid handling in their

Prof. Jones’ and Newton’s results
have just been published in the
Journal of Internal Medicine (2010).
Compared with normal
controls, the patients’ proton
efflux (a measure of acid handling)
was reduced immediately after
exercise (see the figure
opposite), while their time
taken to reach maximum
proton efflux was
significantly prolonged, and
the magnitude of maximum
proton efflux was reduced
compared with the
controls. Taken together,
these findings point to a
significant impairment of proton
excretion in the recovery phase
following exercise — in simple
terms, ME/CFS patients recovered
substantially more slowly than controls.
Could simple deconditioning be the
cause? Probably not, since both
maximum voluntary contraction
measurements and muscle volume
were similar in patients and in the
inactive controls. Rather, the
researchers think it more likely that
impaired acid handing could be one of
the mechanisms through which
autonomic abnormalities act to produce
post-exercise symptoms and fatigue, given
the role played by the autonomic nervous
system in the regulation of acid
transporter pathways and vascular flow in
muscle.
Despite the key role of postexercise symptoms in the illness,
there has actually been very little
scientific investigation into
muscle physiology during
exercise in ME/CFS — a fact that
makes these novel findings so
important. Based on these
results, ME Research UK has
now organised funding for the
next step: an examination of the
function of an energy-generating
enzyme which might be underperforming in people with
ME/CFS (see opposite).

These findings point to a
significant impairment of proton
excretion following exercise
soleus and gastrocnemius muscles during
exercise, which involved raising and
lowering the foot under very controlled
conditions. Measures of autonomic
function were also assessed.

Prof. Julia Newton and Prof. David Jones

6 • BREAKTHROUGH • Autumn 2010

Muscle proton efflux was reduced
in patients after exercise

Controls

Patients

Focusing on muscle:
next steps in Newcastle
In the historical literature, the hallmark of myalgic
encephalomyelitis (ME) has been marked muscle fatigability
often in response to minor degrees of exercise. Muscle cramps,
twitching and extreme muscle tenderness were also common
findings. And today, patients diagnosed with ME/CFS frequently
highlight the importance of peripheral “fatigue”, such as
impairment of muscle power, in their experience of illness. So it
makes sense for researchers to focus on muscle.
Given their results published this year in the Journal of
Internal Medicine, the next step for Prof. Jones and his
colleagues is to see whether a problem with muscle
“bioenergetics” might be at the root of the slower recovery
from exercise seen in ME/CFS patients. For instance, it might
be that acid build-up during exercise is the result of an underperforming energy-generating enzyme within the mitochondria
(the “batteries of the cell”). To investigate this, the researchers
will undertake a range of in vitro studies, all based on primary
assay and culture of muscle cells (myocytes) in the laboratory,
using cells harvested from ME/CFS patients and from matched
normal and chronic disease controls.

The first phase of the investigative strategy has already
been funded by the Northern Clinical Network in
Newcastle, and involves an examination of the function of
ME/CFS patients’ cultured muscle cells; the muscle biopsies
taken during this phase represent a unique opportunity to
study the pathways of metabolism within muscle, exploring
the expression of the key energy-generating enzymes and cell
proteins which help to control acid build up within the cell.
The second phase has been funded by ME Research UK
and involves array studies to look at metabolic gene
expression in muscle. The aim is to show whether cultured
muscle cells from patients with ME/CFS have altered gene
expression, and whether the response of gene expression to
“exercise in vitro” is impaired in patients’ muscle cultures.
The exciting thing is that this series of interlinked studies
brings together investigators from diverse academic
backgrounds (muscle energetics, muscle cell culture and
nanotechnology development), all members of the Institute
of Cellular Medicine within Newcastle University, and all
applying their skills to the illness ME/CFS for the first time.

Autumn 2010 • BREAKTHROUGH • 7

l
a
c
i
m
e
h
c
s
Bio
e
i
t
i
l
a
m
r
o
n
ab
n
e
r
d
l
i
h
c
in
S
F
C
/
E
M
h
t
i
w
here is a particular
poignancy to illness in
youngsters; the
transformation of a
bright, active child into
one who is unable to go
to school or play with friends is
something that touches us all.
Estimates of the numbers of children
affected by ME/CFS vary, but with
prevalence figures of 60 to 70 cases per
100,000, it is likely that around 9,000
people under the age of 16 in the UK
have this diagnosis. As the report to the
Chief Medical Officer in 2002 made clear,
this illness “represents a substantial problem
in the young” and “potentially threatens
physical, emotional, and intellectual
development of children and young people,
and can disrupt education and social and
family life, at a particularly vulnerable time of
life”.
In a previous issue of Breakthrough
(issue 11, Spring 2010), we reported the
results of a study on the quality of life of
children with ME/CFS, recently published
in Pediatrics by Dr Gwen Kennedy of the
Vascular and Inflammatory Diseases
Research Unit in the University of
Dundee. In parallel with this work, Dr
Kennedy and her colleague Dr Faisel Khan
have been investigating biochemical and
vascular abnormalities in children with the
disease, and their results have just been
published in the US journal Archives of
Pediatrics and Adolescent Medicine. Like the
previous study, this work was supported
financially by ME Research UK, The Young
ME Sufferers (Tymes) Trust, Search ME
and Tenovus Scotland.
The Dundee group has previously
reported a number of biochemical and

T

8 • BREAKTHROUGH • Autumn 2010

vascular abnormalities in adults with
ME/CFS. These mainly involve the immune
and cardiovascular systems, and include an
increase in the programmed death
(apoptosis) of white blood cells, raised
levels of oxidative stress which can
damage blood vessels and other organs,
increased markers of inflammation, and
abnormalities in blood vessel function. All
of these are potentially associated with a
future risk for cardiovascular problems
such as heart disease and stroke.
Drs Kennedy and Khan wanted to
investigate whether these abnormalities
were also present in children with
ME/CFS, given the potential long-term
consequences. Risk factors such as high

cholesterol and increased blood pressure,
which are usually associated with adult
diseases, have also been found in children.
These progress into adulthood as
hypercholesterolaemia and hypertension,
so it is important that risks are identified
as early in life as possible.
Twenty-five children with ME/CFS (all
between the ages of 10 and 18 years) and
23 healthy children matched for age,
gender and stage of puberty were
recruited from throughout the UK. The
diagnosis of ME/CFS had been made
according to a revised version of the
CDC-1994 case definition, and was
confirmed by the researchers from a
clinical examination.

Dr Gwen Kennedy

Numbe

r of

White

blood c
ells
undergo
ing apo
ptosis

A blood sample was taken from each
child (using an anaesthetic cream to
minimise their discomfort), and this was
then subjected to a battery of tests in Dr
Kennedy’s laboratory (see the box
overleaf). The child’s blood pressure was
measured, and then the pulse at their
wrist was detected using a special pen-like
probe applied lightly to the skin. This
records the fluctuations in pressure as
each pulse travels along the artery, and is
exactly what you feel with your finger
when you take your own pulse. This
recording of the pulse is then analysed on
a computer to give information on how
flexible the artery is, which gives an
indication of its health and function.
Overall, compared with healthy
control children, the young people with
ME/CFS had:
1. Higher levels of oxidative stress,
manifested as elevated levels of
isoprostanes.
2. Reduced levels of vitamins C and E.
3. A greater percentage of white blood
cells undergoing apoptosis (see the
graph above).
4. A trend towards increased arterial
stiffness, although this was not
statistically significant.

As Dr Kennedy points out, the
increased oxidative stress may be due to a
deficiency of antioxidants in the diet (such
as vitamins C and E, found to be reduced
in this study). However, she feels it is
more likely to have been caused by white
blood cells releasing an excessive amount
of highly reactive free radicals, possibly
from exercising muscle. This would tie in
with the finding of increased white cell
apoptosis, and Dr
Kennedy has
previously
reported
increased
oxidative
stress
following
exercise in
adults with
ME/CFS. She
does emphasise,
however, that more
studies, perhaps including an assessment
of diet, are needed to determine this
mechanism.
The increased apoptosis (or
programmed cell death) may be caused by
a number of factors, including a persistent
viral infection or toxic agent, or an
abnormal immunological response. This

finding is particularly intriguing given that
many patients, including most children in
this study, report that their disease
started following a viral infection of some
kind.
At present however, there is
insufficient evidence to make a causal link
between infection and increased
apoptosis, though the finding is tantalising.
Although there were no other
statistically significant
changes in the
children with
ME/CFS, there
was a
clustering of
markers such
as arterial
stiffness and
cholesterol that
showed small
changes which
may indicate the
possibility of future cardiovascular risk.
This type of clustering has been shown
before in healthy children and in young
people with diabetes. Although it should
be stressed that children with ME/CFS are
at no immediate risk of developing
cardiovascular problems, we might expect
these changes to become greater (closer

Children with
ME/CFS have an
abnormality in the
behaviour of their
immune cells

Autumn 2010 • BREAKTHROUGH • 9

Biochemical measurements
Oxidative stress

to the adult pattern) as the children grow
older and have been ill for longer.
Dr Kennedy and her team conclude
their report by saying that the findings
show that many children with ME/CFS
“have an underlying, detectable abnormality
in the behaviour of their immune cells,
consistent with an activated inflammatory
process”, and provide evidence of “a
persistent or reactivating viral infection
triggering apoptosis of white blood cells with
an increased production of free radicals”.
It is important that these
abnormalities have now been recognised
in children with ME/CFS. To date, aside
from symptomatic treatments, no specific
therapy is available for children or adults
with ME/CFS, so there is an urgent need
for intervention trials. Based on these and
other biomedical findings in the disease,
putative therapies could perhaps include
both pharmacological and nonpharmacological strategies (to treat
dysautonomia, for example), or
antioxidant or antiviral interventions.

Oxidative stress is damage caused by highly reactive molecules called free
radicals. They are normally kept under control by natural processes which
remove them from the circulation, but when an imbalance occurs they can be left
to cause damage unchecked. In particular, free radicals can change our normal
“good cholesterol” into something more harmful, leading to heart and circulation
problems. This “bad cholesterol” is known as oxidised low density
lipoprotein. The reaction of free radicals with essential fatty acids (which are
important substances obtained from the diet) produces compounds called
isoprostanes, which act as another marker of oxidative stress. Other signs of
oxidative stress include low levels of vitamin C and vitamin E.

Inflammation
Inflammation is a complex set of immunological and vascular processes which
occur in response to injury or infection. Although it is a vital part of our body’s
defence mechanism, prolonged inflammation can be harmful to otherwise healthy
tissue, and causes diseases such as rheumatoid arthritis. In particular, it can cause
damage to blood vessels leading to cardiovascular disease. C-reactive protein
is found in the blood and its levels rise in response to inflammation, making it a
useful marker.

Apoptosis
Apoptosis is the programmed destruction of unwanted cells in the body. It is an
important process removing cells that have reached the end of their natural life,
as well as controlling infections. Apoptosis is carried out by white blood cells
called neutrophils, which are part of the immune system. Increased apoptosis can
be a sign of abnormalities in the immune system, and may be caused by a
persistent viral infection or quicker-than-normal turnover of neutrophils.
Apoptosis can be measured by looking at the expression of the protein annexin
V and other substances on the surface of neutrophils. This gives an indication of
what proportion of these cells are healthy, dead because of external factors, or
dead because of apoptosis.

Financial support for this project
The Tymes Trust

Search ME

Tenovus Scotland

The Young ME Sufferers (Tymes)
Trust is the longest-established UK
service for children and young people
with ME and their families. It runs an
advice line, provides access to ME
experts for doctors, teachers and
social workers, and produces a
magazine for children, families and
professionals. The Trust played a
major role in producing the children’s
section of the Department of Health
Report on CFS/ME (2002). See their
website www.tymestrust.org for
details and free publications.

Search ME, based at Rosyth in Fife, was
founded in 2002. Its aims are to improve
the lives of people with ME and to
provide them with a voice on the Cross
Party Group for ME in the Scottish
Parliament. The charity has raised the
bulk of its donations through organising
rock and pop concerts. Search ME
became an early supporter of the work at
the University of Dundee and helped fund
the research carried out there. Further
information can be found on their website
www.search-me.org.uk.

Tenovus has been supporting
innovative medical research within
Scottish Universities and Teaching
Hospitals for over 40 years. It raises
funds through private donations,
Trusts, legacies and fundraising events,
and its principal aim is to assist young
research staff with small grants to get
their research programmes underway.
Find out more at their website
www.tenovus-scotland.org.uk.

10 • BREAKTHROUGH • Autumn 2010

ME Research UK
The first 10 years
The people who gathered for lunch at
Murrayshall House Hotel in rural
Perthshire on 3rd October 2010 were
there at their own expense to celebrate
the 10th Anniversary of ME Research UK
(the photo below shows staff, volunteers
and family members).
The charity was founded in 2000 by
Dr Vance Spence, Robert McRae and
Roger Jefcoate CBE (who became
founding patron), all of whom realised
something had to be done to promote
and fund research into ME/CFS. As Vance

says, “Good scientific research into ME is
vital, but looking around we saw that basic
biomedical research was grossly underfunded.
If money and resources could be found, then
the tectonic plates might start to move. We
were also concerned that the research picture
was heavily skewed towards psychiatry and
psychology, an odd business since Bob and I
had a physical illness and had no
psychological problems.”
With the support of our patrons The
Countess of Mar and Dr Gordon Parish,
the organisation has grown in size and

respect over the decade, punching above
its weight in a variety of spheres.
The trustees have bold plans for the
future, based on the small, committed
team of core staff, an advisory panel of
professional scientists, and a group of
trusted volunteers who help the charity
to run efficiently. From this strong start,
the whole team are committed to
establishing ME Research UK as a major
force for change that will make a real,
long-term difference to the lives and
prospects of people with the illness.

Autumn 2010 • BREAKTHROUGH • 11

A decade of research
Over the past 10 years we have funded
the work of a number of scientists in the
UK and overseas, whose research covers
several different areas of interest.
Funding was provided for 29 specific
investigations on ME/CFS patients (some
of which are listed on the right), and we
are particularly grateful to some of the
ME organisations which have provided
larger donations to help us fund specific
projects.

Dr Gwen Kennedy

Dr Jo Nijs

Dr Ellie Stein

An example of
consistent funding
Unravelling the scientific basis of ME/CFS,
or the collection of diseases currently
given that label, is no simple matter.
Funding one-off investigations is useful
since these can provide pilot data for
subsequent grant applications, or spark off
interest in other researchers.
But in modern science, real
breakthroughs come at the end of a
programme of painstaking work by a
specialist group of researchers. One of
the few examples of such a programme
on ME/CFS, anywhere in the world, is the
work at the Vascular Diseases Research
Unit, University of Dundee.
This group has received a number of
grants from ME Research UK in the past
10 years. In a step-by-step progression
involving both adults and young people
with the illness, the group has uncovered
a number of abnormalities.
Ÿ Unusual sensitivity of blood flow to
acetylcholine (a neurotransmitter).

Dr Jonathan Kerr

12 • BREAKTHROUGH • Autumn 2010

Our priority has always been to
support innovative clinical and biomedical
studies, based in established research
institutions, investigating the causes of
ME/CFS and the effectiveness of potential
treatments. All our grants are competitive
and are subject to peer review. Fuller
details of these and other projects,
including the key findings published in
scientific papers, can be found at the
research section of our website.

Ÿ Increased levels of isoprostanes (a
gold standard marker of oxidative
stress in the bloodstream).
Ÿ An unexpected increase in dying
(apoptotic) white blood cells,
consistent with an activated
inflammatory process or persistent
infection.
Ÿ Increased cardiovascular risk factors
with arterial stiffness in patients.
Ÿ Biochemical anomalies in children
mirroring those found in adults with
the illness.
Such a progression — whether
towards positive findings or away from
negative ones — is the norm for scientific
investigation.
The burning need in this illness is for
there to be many groups undertaking
programmes of research across a range of
basic and clinical science fields, so that a
‘critical mass’ of investigators can produce
a ‘critical mass’ of biomedical data.

Vitamin D supplementation and cardiovascular disease risk
Dr Faisel Khan, Institute of Cardiovascular Research, University of Dundee
Autonomic nervous system dysfunction — a clinical study
Prof. Julia Newton, School of Clinical Medical Sciences, University of Newcastle
(with cofunding from the Irish ME Trust and the John Richardson Research Group)
Interleukin-6 and its receptors
Prof. Myra Nimmo, University of Strathclyde, Glasgow

Prof. Jonas Blomberg

Biochemical and blood flow aspects in children
Dr Gwen Kennedy, University of Dundee
(with cofunding from The Young ME Sufferers Trust and Search ME)
Evaluation of pain and therapeutic interventions
Dr Lorna Paul and Dr Les Wood, Glasgow Caledonian University
Gene expression studies
Dr J Kerr, St George’s Hospital, University of London
(co-funded by the Irish ME Trust)
Non-invasive neuroimaging of the brain
Prof. BK Puri, Imperial College London
(with co-funding from ME Solutions and the MRC Clinical Sciences Centre, Imperial College)

Raising awareness
The first 10 years
ME Research UK’s mission to “Energise
ME Research” involves raising awareness
of the need for biomedical research to a
variety of audiences, hosting conferences
and meetings, and providing high quality
information on all aspects of the illness:
from summarising and appraising scientific
literature on ME/CFS to informing the
policy agenda. Here are some of our key
achievements.

XPG at Scottish Parliament
We provided the impetus and initial
funding for the formation of a Cross Party
Group on ME at the Scottish Parliament.

Informing policy
Formal representations to official bodies
have included: Royal Society of Medicine
(2009); National Institute for Clinical
Excellence (2006–7); Gibson Westminster
Parliamentary Inquiry (2006); Royal
College of Paediatrics and Child Health
guidelines (2006); and Scottish Parliament
(2001 and 2005).

Scientific meetings
We have hosted two New Horizons
International Research Conferences
(Edinburgh 2007 and Cambridge 2008); a
Research Colloquium (2007); and a
Research Workshop (2005).

Royal visit
In 2009, we were honoured with a visit
from His Royal Highness The Prince
Edward, who met the team and was
introduced to our work.
Talks and presentations
Dr Vance Spence gave some 58 public
talks on ME/CFS research and related
issues in ten years, at venues ranging from
Sheffield and Southampton to Dumfries
and Dublin.

DVDs produced
A DVD lecture by Dr Vance Spence on
research issues and challenges was made,
and 3,000 copies distributed. We also
produced films of our conferences.
Books and key articles
“Shattered — Life with ME” (Thorsons)
by Dr Lynn Michell, an early trustee of the
charity, was produced and distributed.
And a plethora of specialist articles have
been written for the magazines of local
and national ME organisations (see the
information section of our website).
14 • BREAKTHROUGH • Autumn 2010

Breakthrough magazine
We have developed Breakthrough into a
full-colour bi-annual magazine featuring
research and comment, with a readership
of almost 7,000.
Website
Our website, which also contains our
research database, has become a source
of information for researchers, health
care professionals and people with the
illness across the world.

XMRV: the plot thickens
In October 2009, a scientific
paper in the prestigious journal
Science reported the discovery
of a potential retroviral link to
ME/CFS, which is estimated to
affect some 17 million people
worldwide.
The consortium of
researchers, including the
Whittemore Peterson Institute
(WPI) located at the University
of Nevada, USA, had found that
DNA from xenotropic murine
leukaemia virus-related virus
(XMRV) could be detected in
the peripheral blood
mononuclear cells of 67% of
ME/CFS patients compared with
only 3.7% in controls, and that
XMRV proteins were being
expressed in blood cells from
ME/CFS patients at very high levels
compared with controls.
Since the presence of infectious
XMRV in white blood cells of patients
could account for some of the known
features of this chronic illness (e.g.,
neurological symptoms and immune
dysfunction with inflammatory cytokine
upregulation), the finding was tantalisingly
appropriate. However, scientific results
must be confirmed by others, and the
crucial first step is for other independent
laboratories across the world to look for
XMRV infection in their own local
populations. So ME Research UK (along
with the Irish ME Trust) quickly provided
funding for researchers to test Swedish
ME/CFS patients (see the Spring 2010
issue of Breakthough).
In the ten months following the initial
report, four other studies have been
published, all “negative” for the presence
of the virus in English, Scottish, Dutch and
American patients. At first glance, these
negative reports from four different
research groups across the globe, each
with a track record in virology, is a
serious blow to hopes of XMRV
involvement in ME/CFS.
However, the situation is more
complex, and the past few months have
seen an intense discussion of intricate
methodological issues. As Dr Robert

Silverman, the discoverer of the XMRV
virus, makes clear in an excellent review
(Nature Reviews Urology, July 2010), there
might be several reasons — apart from
plain contamination, which is unlikely —
for radical differences between studies.
First, there could be geographical
differences in the distribution of XMRV,
as is the case with another human
retrovirus, HTLV-1. Next, sequence
variations in XMRV, and the existence of
divergent or related viruses, is possible,
and these could easily be missed by many
of the methods, in particular protein chain
reaction (PCR).
Also, the absence of standardised,
highly sensitive methods for the detection
of XMRV, coupled with a lack of widely
available, positive control human samples,
might be contributing to the different
results obtained between studies. This last
point is important, particularly if XMRV is
indeed hard to detect by the conventional
PCR methods used in the four negative
papers; a recent scientific article
(Virulence, Sep/Oct 2010) has proposed
four additional blood-based lab assays for
more sensitive detection of XMRV.
Then, in a dramatic twist to the story,
Dr Harvey Alter of the National Institutes
of Health published a report in Proceedings
of the National Academy of Sciences (23rd
August 2010). His team were examining

long-stored samples from 37
CFS patients for traces of the
XMRV “gag gene”. But instead of
finding XMRV itself, they
uncovered a more diverse group
of closely related viruses;
startlingly, these were present in
86.5% of the patients but only
6.8% of the control samples.
The researchers claim that
the diverse viral sequences
identified closely resembled the
polytropic mouse viruses (those
infecting a range of hosts
including mice), which is why
they adopted the term “MLVrelated virus” (see the box
below). However, Dr Alter
pointed out that his work
supports the original report in
Science in 2009 since XMRV is a
subset of MLVs, although his team did not
precisely replicate the work in the original
study.
Whether or not MLV-like viruses
play a critical role in ME/CFS, the scientific
twists and turns of the past year have
been absorbing and compelling, and more
are yet to come.

What are MLVs?
Murine leukaemia viruses (MLVs)
are gammaretroviruses capable of
causing mouse (murine) cancer.
There are many types of MLVs,
most used in cancer research (for
example, specific genes can be
delivered to target cells by MLVderived particles).
XMRV is part of the MLV “family”,
but an unusual one because it can
infect other non-mouse species —
hence its name “xenotropic”.
Dr Alter reported evidence for
three different variants of MLV in
ME/CFS patients, though one
predominated, infecting 86% of
patients.

Autumn 2010 • BREAKTHROUGH • 15

Recent research from
around the world

CHICAGO
Indomitable spirit
While recovery from ME/CFS is a real
possibility, particularly in the young, many
people still remain chronically ill for a
number of years coping as best they can.
Healthcare professionals recognise a
number of different “strategies” for
coping with chronic illness, ranging from
self distraction or denial or self-blame to
humour or religious faith. So, which
strategies are most often used by ME/CFS
patients, and does length of illness make
any difference to how they cope?
Researchers from DePaul University,
Chicago (writing in Psychological Reports)
compared coping strategies between
ambulatory adult patients with a longer
(more than 2 years) or shorter (2 years
or less) duration of illness. Patients’ levels
of illness and symptoms were assessed,
and the Brief COPE inventory was used
to identify their ways of coping.
Interestingly, there were no
differences in physical impairment or
symptom severity between the two
groups. But people with a longer duration
of illness were more likely to use
16 • BREAKTHROUGH • Autumn 2010

strategies such as active coping (e.g.,
“taking action to try to make the situation
better”), positive reframing (“looking for
something good in what is happening”),
planning (“thinking hard about what steps
to take”) and acceptance. And they were
less likely to use behavioural
disengagement (such as “giving up the
attempt to cope”) than people ill for a
shorter time.
The key finding that patients show
improvements in coping over time,
regardless of their physical function or
symptoms, illustrates one thing: the
indomitable power of the human spirit in
coming to terms with a dreadful clinical
and social situation.

BATH
Subgroups
in children
There are some 13 million people in the
UK under the age of 16, and we’re told
that around 9,000 (0.07%) of them have a
diagnosis of ME/CFS. But what does that
mean? Do they all have the same
underlying disease or might there be a

collection of different illnesses in this
diagnostic black box?
To investigate this, the Bath specialist
paediatric service which covers the southwest of England decided to review its data
on children assessed between 2005 and
2008. The team employed factor analysis,
a statistical technique that uses
correlations between symptoms to
determine individual “factors” that might
hypothetically correspond to pathological
disease processes, and might identify
clinically differentiable subgroups
(“phenotypes”) of children. Analyses were
performed on the symptoms reported at
initial assessment by 333 children and
young people (average length of illness 17
months, 40% attending school), and
regression analyses included variables
such as sex, age, length of illness, anxiety
and markers of severity (fatigue, physical
function, pain and school attendance).
The scientific report (published in
Archives of Disease in Childhood) identified
three different clinical “phenotypes”,
described under the broad headings of
musculoskeletal, migraine and sore throat.
The musculoskeletal subtype was
associated with muscle and joint pain, and
hypersensitivity to touch, and was more
strongly associated with fatigue than the
others. The migraine subtype was
associated with noise and light
hypersensitivity, headaches, nausea,
abdominal pain and dizziness, and it also
had the strongest association with lower
physical function and worse pain than the
other phenotypes. The sore throat
subtype was associated with sore throat
and tender lymph nodes. This appeared to
be the least severely affected group, and
was associated with female gender but
not with fatigue or pain. Interestingly,
neither age, length of illness or symptoms
of depression seemed to affect phenotype
classification.
While factor analysis cannot prove the
existence of separate illnesses sheltering
under the umbrella term “ME/CFS”, the
finding that three phenotypes can be
clearly differentiated from each other in
children with the diagnosis is certainly
suggestive.

MIAMI
Natural born killers
Ask any person with ME/CFS what
advance in research they would most like
to see, and surely a diagnostic test or
marker for the disease would come near
the top of the list. Genetics might appear
to provide the greatest hope in achieving
this goal, but there are other options, as a
team of researchers from the University
of Miami have recently demonstrated.
Their work (published in PLoS One)
has focused on two potential markers that
are thought to be involved in the
development of ME/CFS. First, natural
killer cells, which are a type of white
blood cell responsible for killing other
cells; they are important in the body’s
immune defence against tumours and viral
infections, but their function appears to
be deficient in ME/CFS. Second, dipeptidyl
peptidase IV (also known as CD26), which
is an enzyme also involved in immune
regulation and programmed cell death,

and which has previously been found to
be a marker for various types of cancer.
The levels of this enzyme on lymphocytes
(white blood cells) has also been shown
to be increased in people with ME/CFS.
The Miami study found that the
cytotoxic function of natural killer cells
was significantly lower in 176 ME/CFS
patients than in 230 healthy controls.
Also, the proportion of lymphocytes
positive for CD26 was higher in the
patients than in the controls, while the
levels of CD26 expressed on T cells and
natural killer cells and in the blood was
lower. Taken together, these observations
are consistent with the idea that infection
is involved in the initiation and/or
persistence of ME/CFS.
Could natural killer cells’ cytotoxicity
and CD26 expression, or a combination,
become useful as objective markers for
diagnosis or treatment targeting? Well, as
you read this sentence, the researchers
are engaged in the next phases of their
work, looking at how these markers
change throughout the illness, to answer
that very question.

UTAH
Gene expression
during exercise
The cardinal symptom of ME is profound,
post-exertional loss of muscle power
associated with muscle pain, tenderness
and swelling, and “post-exertional”
symptoms are still key to diagnosis. Even
the imperfect NICE Clinical Guideline of
2007 insists that post-exertional malaise
should be present. Experimental studies
of the effects of exercise in patients are
therefore vital, and a recent report
(published in the Journal of Pain) has
examined gene expression 8, 24 and 48
hours after a 25-minute bout of wholebody exercise involving a combined armleg cycle ergometer.
ME/CFS patients, but not healthy
controls, reported increased physical
fatigue up to 48 hours after the exercise
bout, and only this group showed
significantly increased levels of pain and
increased mental fatigue up to 48 hours.
But the gene expression results were the
most interesting. With this moderate
exercise task, the 16 healthy control
subjects exhibited no significant increases
in expression of any of the genes, whereas
the 19 ME/CFS patients showed increases
in the expression of a variety of genes.
Overall, the patients showed greater
increases than healthy people in genes
that can detect increases in muscleproduced metabolites (ASIC3, P2X4 and
P2X5), genes that are essential for
sympathetic nervous system processes
(adrenergic b-2A, b-1 and b-2, as well as
COMT), and immune function genes (IL10
and TLR4) — increases that were
observed to last from 30 minutes to 48
hours. In the subgroup of ME/CFS patients
who also had fibromyalgia, these increases
were highly correlated with symptoms of
physical fatigue, mental fatigue and pain.
Given that approximately 90% of the
ME/CFS patients could be distinguished
from healthy controls using four of the
genes measured (P2X4, b-1, b-2 and
IL10), it may be that alterations in gene
expression from circulating white blood
cells after exercise could come to be used
as objective markers for the illness,
although much more work would be
required to establish this with certainty.
Autumn 2010 • BREAKTHROUGH • 17

Cognitive deficits in patients with ME/CFS

AUSTRALIA
Memory and
attention problems
Neurocognitive problems are one of the
most frequent and disabling symptoms
associated with ME/CFS. In one
investigation, 89% of patients reported
memory/concentration problems, while in
another large study memory/attention
deficit problems were reported by
approximately 90% of 2,073 consecutive
patients. Crucially, patients often report
that their cognitive problems can be made
worse by physical or mental exertion. But
do such self-reported anecdotes about
cognitive symptoms also show up as
measurable deficits on objective cognitive
testing in a clinical setting?
Meta-analysis is a method of
combining results from a range of studies
to obtain an overall estimate of the “true”
18 • BREAKTHROUGH • Autumn 2010

effect of a treatment. Researchers at the
University of Adelaide, South Australia
have just published (in Psychological
Medicine) a meta-analysis of all relevant
clinical trials examining cognitive
functioning in people with ME/CFS, with
the aim of identifying the pattern and
magnitude of these deficits. Overall, they
found a very mixed bag of 50 studies
(made up of 1,577 patients and 1,487
controls) published between 1988 and
2008 from which, nevertheless, a clear
and very revealing pattern emerged on
detailed examination.
The most significant cognitive deficits
(see the chart above) were found in
“attention” (encompassing attention span
and working memory), “memory”
(examined from verbal and visual memory
tests, mostly memory for word lists) and
reaction time (assessed as responses to
both simple and complex choice stimuli).
These results were consistent with the
memory and concentration problems that
patients themselves complain about. In

contrast, there were no apparent deficits
on tests of “fine motor speed”,
“vocabulary”, “reasoning” or “global
functioning”, suggesting that the “higher
order” cognitive abilities such as language,
reasoning and intelligence remain
unimpaired. Importantly, most studies that
examined the impact of self-reported
depression on cognitive functioning failed
to find a relationship, indicating that
depression was not responsible for most
cognitive impairments.
The range of these studies and the
clarity of the findings leave no doubt that
people with ME/CFS have moderate to
large impairments in simple and complex
information processing speed, and in tasks
requiring working memory over a
sustained period of time. As the authors
point out, the deficits in performance are
around 0.5 to 1.0 standard deviations
below that of healthy people, a fact which
explains the significant impact cognitive
problems have on patients’ day-to-day
activities and quality of life.

CHICAGO
Medical text books
To a patient with ME/CFS, the attitude of
their general practitioner towards the
illness can have a big impact on how
quickly they are diagnosed, how
sympathetically they are treated, and their
access to healthcare services. Yet we
know that a large percentage of GPs
(roughly half in one 2005 study) don’t
believe the condition actually exists —
despite official and authoritative
confirmation of the reality and
seriousness of the illness by various
reports, such as the 2002 CMO report
and the 2007 NICE guideline. And we
know from phone calls to the charity that
patients on the ground can struggle to
find an understanding doctor willing to
take their illness seriously.
Medical education has a role to play
in forming attitudes, particularly text
books which, though not usually as up-todate as articles in scientific journals, are
often also used as a source of references
and reviews. One group at DePaul
University in Chicago recently set out to

understand more fully how ME/CFS is
represented in medical text books. They
selected a total of 119 mostly US
published books in a variety of areas
(including immunology, pathology, internal
medicine and psychiatry), and reviewed
the number of pages mentioning “CFS”
and whether that information included
any mention of aetiology, classification,
diagnosis, recommended treatments or
prevalence. Importantly, they also noted
whether the text specifically mentioned
the term myalgic encephalomyelitis, “ME”.
Their results (published in the
Australian Journal of Primary Health) are
unsurprising and disheartening. Only
40.3% of the books they reviewed
included any information on “CFS”, and
only 16% had any mention of “ME”
terminology — far smaller proportions
than for other less prevalent illnesses,
such as multiple sclerosis (57%) and Lyme
disease (55%). In fact, the topic took up a
paltry 116.3 pages (0.09%) of the 129,527
total reviewed.
Of course, less is known about
ME/CFS than these other conditions, but
even so, these books might have been
expected to cover an illness estimated to
affect between 400,000 and 900,000
people in the USA, which is where most
of the textbooks were published. Such
chronic under-representation of ME/CFS
in medical textbooks surely serves to
reinforce, and possibly legitimise, the
prevailing scepticism about
this condition.

LONDON
A FINE surprise?
From 2003 to 2009, the vast bulk of the
£3.1 million spent by the Medical
Research Council on ME/CFS research
went into two clinical trials.
The largest was the PACE trial which
compared cognitive-behavioural therapy
(CBT), graded exercise (GET) and pacing,
and which has yet to report its results.
The other study was the FINE (Fatigue
Intervention by Nurses Evaluation) trial in
which severely affected patients were
randomly allocated to one of three
treatment groups: “pragmatic
rehabilitation”, a nurse-led self-help
approach which included elements of CBT
and GET delivered in the patients’ homes;
supportive listening; or usual care
provided by their GP.
The first results of the FINE trial, the
cost of which exceeded £820,000, were
reported recently in the British Medical
Journal. A total of 296 adults with ME/CFS
were enrolled, and after 20 weeks of
treatment, patients receiving pragmatic
rehabilitation were significantly less
fatigued and depressed, and were sleeping
better than those who received usual care
(although there was no difference in
physical functioning).
However, when the participants were
seen one year later there was no longer
any difference between these two
treatment groups. Thus, while pragmatic
rehabilitation appeared to help fatigue and
depression in the short term, over a
longer period it was no better than usual
care provided by a GP (with supportive
listening having no extra benefits at all).
Are these negative results a surprise?
Not really, given that pragmatic
rehabilitation does not, and was never
intended to, address the pathophysiological basis of disease in these
severely ill people.
The real surprise (which is discussed
more fully in the July 2008 issue of
Breakthrough) is that most of the MRC’s
inadequate grant-spend on ME/CFS has
gone to fund trials of non-specific
management and coping strategies, at the
expense of truly biomedical research —
the reverse of the situation in other
illnesses such as multiple sclerosis or
rheumatoid arthritis.
Autumn 2010 • BREAKTHROUGH • 19

The
Friends
in
`` Hard
A
'
Days
''
Fundraising
Tribute Act Concert
Amy and Sue Bakewell were interviewed by BBC Radio Leicester
at the time of the tragic case of Lynn Gilderdale, since Amy is
very seriously affected with ME and has lived in isolation in her
dark bedroom for 14 years. After this, the presenter visited Amy
and offered to organise a charity concert to raise funds for ME
research, an offer the family couldn’t refuse.
The performances at the concert were all tribute acts: The
Fib Four as the Beatles, Micky Vegas as Elvis Presley, and Cliff-AsIf as Cliff Richard. They all gave a super evening’s entertainment
at Thornton Working Mens Club, and the extremely wellsupported event raised £850.
Sue explains, “Two days before the concert on 12th May, ME
Awareness Day, BBC Radio Leicester broadcast its mid-morning show
from our village shop. It was great fun, incorporating interviews with
customers, our local ME support group, and Amy. We were pleased to
be helping to raise the profile of ME with this excellent publicity.”

Pyjamathon
To mark ME Awareness Week 2010, Annalisa McGorlick wore
nothing but pyjamas for 7 days (as proved above)!
She explains, “At the risk of being locked up, I went around in
pyjamas, indoors and outdoors, rain or shine, to the pub, to the
supermarket and everywhere else. I had to do something, since our
government puts £0 into biomedical research for this illness, but
without financial backing research cannot be carried out and this
life-destroying illness will continue to go untreated and unrecognised.”
Annalisa’s ME symptoms became severe at age 16, and now
after a long, hard journey and various treatments, she is able to
live a semi-normal life and to go out a few times a week —
hence the “Pyjamathon”. She was very pleasantly surprised with
the public reaction which was one of support and intrigue, and
raised £240 from the event.

Bucket collections
The aficionados of the Worcestershire
ME Support Group, Pauline and Mike
Pearson and Warwick Davis (pictured)
got together with the Solihull and South
Birmingham ME Support Group to hold
bucket collections for ME Research UK.
In the summer they headed for
Beckett’s Farm Shop at Wythall and
Evesham Country Park shopping and
garden centre with their ME information
stand and buckets, raising over £930.
The group is very active, and its
monthly informal gatherings are held
under the auspices of County Coordinator Jill Pigott. Many thanks to all its
members for supporting this event.
20 • BREAKTHROUGH • Autumn 2010

London Marathon 2010
Virgin London Marathon day was a great festival of fun for everyone involved. ME
Research UK has benefited greatly from London Marathon runners in the past. In 2008,
Robert Ogden, Madhi Choudhury and Ian Bottomley ran for us, as did Harvey Gurry
and Matthew Fielding in 2009. And this year, we were honoured to have two
champions who again used their individual places to run on our behalf.
One of the runners was Dan Plant whose sister had ME some years ago but has
since made a wonderful full recovery, so he wanted to help raise funds for research. He
says, “After a lot of training, I made it on the day and gave it my best shot — something of a
miracle in itself for someone who previously considered lifting a few pints as exercise.”
Our other runner was James Albiges (pictured below), who over the last few
months has seen the debilitating effect of ME first hand so wanted to raise money for a
cause close to his heart. His aim was “to beat 4 hours and then retire gracefully”. Both did
very well: Dan crossed the line in 4.41.20, and James in 3.56.37, beating his 4-hour
target!

Mayor of Hastings
Hastings’ new Mayor, Kim Forward, took
up her post at the annual mayor-making
ceremony in May. Proposing her, a fellow
Councillor said, “Kim relates to all the
people she meets with warmth and genuine
interest in their well-being. These qualities will
be invaluable in her new civic role.” In her
speech of acceptance Mayor Forward
promised to bring energy and enthusiasm,
and to promote the interests of Hastings
and St Leonards, beautiful places which
have so much to offer.
Mayor Forward has chosen to
support three charities in her mayoral
year: the NSPCC, Care for the Carers
and ME Research UK. Her 14-year-old
son has had ME for some time, and is now
able to walk again although his recovery
from the debilitating illness has been slow.
We wish Kim a successful year in
office, and send her our grateful thanks
for choosing us as one of her supported
charities.
Autumn 2010 • BREAKTHROUGH • 21

Run, Simon, Run!
Simon Patchitt’s Bristol 10k run during
ME Awareness Week was a great success.
“It’s the first time I’ve been in any kind of
race since sports day in 1994,” says Simon,
who crossed the finish line in 56 minutes
and 38 seconds. “I really enjoyed it, even
though I needed oxygen in the medical tent
afterwards!” (As it turned out, the nurse
remembered him from school!)
Linda, Simon’s girlfriend, has had ME
for almost 10 years. She says, “Many
sufferers (like me) are severely affected, but
because they often can’t go out, no one sees
them, so nobody realises how ill they are.”
She saw the run as a great chance to raise
awareness about the impact of ME.
Linda and Simon collected £1,085
from the event — more than double their
target. “We’re so pleased; thanks to
everyone who sponsored the run.” Since the
race, Simon has kept up the running and
has entered the Bristol half marathon in
September.

Greg loses his hair
Greg Carslaw from Birmingham promised
himself that he’d wait a decade before
getting a haircut. But after 8 years he
thought a trim might be nice, and his
friends suggested that they might even
donate money to charity to see it cut.
But the deal was complex. If he
managed to raise £100, Greg would cut
off half his hair (head, beard, eyebrows,
nasal-hair, whatever). But after that, for
every £41.26 raised (amount selected by
arbitration) he’d shave off half his
remaining hair. This meant that if
everyone he knew offered up a fiver, he’d
be left with one eyebrow. As an added
bonus, whichever generous person gave
the most money would have the option
to specify some intermediate cut style
which Greg would have to wear for 24
hours.
The photo shows Siz, eager with the
shears to do a lot of lopping — a threat
she carried out a few days later. Greg
raised over £500, so thanks to him and all
his mates.
22 • BREAKTHROUGH • Autumn 2010

MERUK in the Media
We’ve made quite a fizz in the past 6 months.

Children’s study media coverage
The publication of the University of Dundee’s scientific study of children with ME/CFS
(see page 8 of this issue) got extensive publicity. On 7th September, things kicked off
with Prof. Jill Belch on the BBC Radio 4 Today programme, and continued throughout
the day with regular items on BBC News, BBC World Service and BBC Radio regional
broadcasts, with ITV taking up the cudgels later in the day. At the same time, a plethora
of items appeared across the Internet — on BBC Health, Top News Network USA,
WebMD Health News, Scottish Television, UKwired News and Pharmaceutical Live.
Thereafter, the printed media covered the story widely on 8th September. The
Times kicked off with a half-page “Study proves that the illness is not psychological”,
and there were items in the Herald De Paris, Daily Mail Online, Nursing times, the
Scotsman, the Los Angeles Times, and an editorial in the Lancet.

Broadcasts on Real Radio
Real Radio is part of one of the country’s largest radio stations, and operates across the
UK. For a week from the 16th to 20th August, we had a series of 40-second adverts
highlighting five different cases of ME (one each day) and the need for research into the
illness. For example, Wednesday’s case described “31 year old Liz was teaching biology in
a high school when she got a viral infection and become so ill she was off work for five
months… That was 24 years ago…” These broadcasts have been very well received,
raising awareness of the reality of living day-to-day with ME.

Herald Scotland Opinion Piece
A 600-word opinion piece by Dr Neil Abbot, “Why we need to start treating ME much
more seriously”, was published in the Herald newspaper on 27th July 2010, and can be
read on-line.

If you think your story would make a good subject for similar
programmes and would be happy speaking about your case to
the media, please let us know — we’d love to hear from you
Shop at Amazon for ME Research UK
Can there be any easier way to earn money for our charity? If you are buying from
Amazon, then just click through the link on the Amazon page on our website, and 5%
or more of your purchases could be making its way back to ME Research UK. It really
is that simple.
Whether it’s books, electronics or toys, Amazon has it all. Provided that you
connect to Amazon via one of our links, your shopping will qualify. The amount we get
varies according to the type of product and the type of link followed. It won’t cost you
a penny more, and you won’t lose out on other discounts, so please help us by
shopping via ME Research UK’s Amazon link.
Visit our website for more details: www.meresearch.org.uk/support/shopping.html.